Beta frequency synchronization in basal ganglia output during rest and walk in a hemiparkinsonian rat.
Beta frequency synchronization in basal ganglia output during rest and walk in a hemiparkinsonian rat.
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DOI：
10.1016/j.expneurol.2009.11.016
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发表时间：
2010-02
影响因子：
5.3
通讯作者：
Walters, Judith R.
中科院分区：
文献类型：
--
作者：
Avila, Irene;Parr-Brownlie, Louise C.;Brazhnik, Elena;Castaneda, Edward;Bergstrom, Debra A.;Walters, Judith R.
关键词：
在帕金森氏病患者的基底神经节中观察到β频率范围内的同步振荡神经元活动，并假设是反动力学的。单侧受损的帕金森病大鼠模型可以通过直接比较运动活动中未受损和多巴胺细胞受损半球基底神经节输出的β活性来检验这一假设。在旋转跑步机上训练的单侧黑质纹状体损伤大鼠和对照组大鼠肩胛肌肌电活动记录双侧黑质网状部（SNpr）的单位和局部场电位（LFP）。左半球病变后，大鼠在跑步机上行走困难，但可以在跑步机上行走。在注意力不集中的休息期间，多巴胺缺失半球的SNpr LFP功率在12-25 Hz范围内（低β）显著高于未受损半球和对照半球。在行走过程中，所有半球的低β能量都减少了，而受损半球的25-40 Hz（高β）活动选择性地增加了。左旋多巴减少了高β功率的增加。与未受损半球相比，在多巴胺枯竭半球，SNpr峰值与休息时SNpr低β - LFP振荡和行走时高β - LFP振荡的同步性更为显著。数据显示，多巴胺丢失与休息和行走时SNpr低β范围和高β范围活动的相反变化有关，并表明行走时受损半球SNpr输出高β范围活动的同步增加可能导致半帕金森大鼠的步态障碍。
Synchronized oscillatory neuronal activity in the beta frequency range has been observed in the basal ganglia of Parkinson’s disease patients and hypothesized to be antikinetic. The unilaterally lesioned rat model of Parkinson’s disease allows examination of this hypothesis by direct comparison of beta activity in basal ganglia output in non-lesioned and dopamine cell lesioned hemispheres during motor activity. Bilateral substantia nigra pars reticulata (SNpr) recordings of units and local field potentials (LFP) were obtained with EMG activity from the scapularis muscle in control and unilaterally nigrostriatal lesioned rats trained to walk on a rotary treadmill. After left hemispheric lesion, rats had difficulty walking contraversive on the treadmill but could walk in the ipsiversive direction. During inattentive rest, SNpr LFP power in the 12–25 Hz range (low beta) was significantly greater in the dopamine-depleted hemisphere than in non-lesioned and control hemispheres. During walking, low beta power was reduced in all hemispheres, while 25–40 Hz (high beta) activity was selectively increased in the lesioned hemisphere. High beta power increases were reduced by L-DOPA administration. SNpr spiking was significantly more synchronized with SNpr low beta LFP oscillations during rest and high beta LFP oscillations during walking in the dopamine-depleted hemispheres compared with non-lesioned hemispheres. Data show that dopamine loss is associated with opposing changes in low and high beta range SNpr activity during rest and walk and suggest that increased synchronization of high beta activity in SNpr output from the lesioned hemisphere during walking may contribute to gait impairment in the hemiparkinsonian rat.
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